Abstract

The major consequences of alcoholic cirrhosis, esophageal varices and ascites, emerge years before hepatic failure occurs and are related to portal hypertension. The pathogenesis of elevated portal pressure involves both increased resistance and increased portal blood flow (1). Early in the course of portal hypertension, regardless of cause, portal blood flow increases (2), possibly because of the opening of portosystemic shunts; this increase is associated with a generalized hyperdynamic circulation and peripheral vasodilation.

It has been known for nearly 40 years that patients with cirrhosis have a hyperdynamic circulation associated with increased cardiac output and heart rate, reduced arterial blood